ScienceDaily (Nov. 20, 2007) — Doing the right kind of brain exercise can enhance memory and other cognitive abilities of older adults, according to new research.

Dr. Elizabeth Zelinski of the University of Southern California Andrus Gerontology Center presented data* from the IMPACT study (Improvement in Memory with Plasticity-based Adaptive Cognitive Training) – the largest study ever done on aging and cognitive training using a program available to the public.

ScienceDaily (Nov. 29, 2007) — MIT researchers have shown that a cocktail containing three compounds normally in the blood stream promotes growth of new brain connections and improves cognitive function in rodents.. . .In the Brain Research paper, the MIT team reported that rodents given a cocktail of DHA (a type of omega-3 fatty acid), uridine and choline showed a greatly increased concentration of dendritic spines, which receive messages in the postsynaptic neuron. That indicates that synapse regeneration has occurred, which is unusual, Wurtman said.

Synapse regrowth could also prove an effective treatment for other brain diseases, such as Parkinson's, or for brain injuries, he said.

The researchers found that rodents who received the treatment performed much better on tests of cognitive ability

ScienceDaily (Nov. 29, 2007) — Having hypertension, or high blood pressure, reduces blood flow in the brains of adults with Alzheimer's disease, according to a new study presented today at the annual meeting of the Radiological Society of North America.

It's good news that we are living longer, but bad news that the longer we live, the better our odds of developing late-onset Alzheimer's disease.

Many Alzheimer's researchers have long touted fish oil, by pill or diet, as an accessible and inexpensive "weapon" that may delay or prevent this debilitating disease. Now, UCLA scientists have confirmed that fish oil is indeed a deterrent against Alzheimer's, and they have identified the reasons why.

Reporting in the current issue of the Journal of Neuroscience, now online, Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine at UCLA and associate director of UCLA's Alzheimer Disease Research Center, and his colleagues report that the omega-3 fatty acid docosahexaenoic acid (DHA) found in fish oil increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the protein that forms the "plaques" associated with the disease.

The plaques are deposits of a protein called beta amyloid that is thought to be toxic to neurons in the brain, leading to Alzheimer's. Since having high levels of LR11 prevents the toxic plaques from being made, low levels in patients are believed to be a factor in causing the disease.

Alzheimer's is a debilitating neurodegenerative disease that causes memory loss, dementia, personality change and ultimately death. The national Alzheimer's Association estimates that 5.1 million Americans are currently afflicted with the disease and predicts that the number may increase to between 11 million and 16 million people by the year 2050.

The researchers examined the effects of fish oil, or its component DHA, in multiple biological systems and administered the oil or fatty acid by diet and by adding it directly to neurons grown in the laboratory.

"We found that even low doses of DHA increased the levels of LR11 in rat neurons, while dietary DHA increased LR11 in brains of rats or older mice that had been genetically altered to develop Alzheimer's disease," said Cole, who is also associate director of the Geriatric Research Center at the Veterans Affairs Medical Center.

To show that the benefits of DHA were not limited to nonhuman animal cells, the researchers also confirmed a direct impact of DHA on human neuronal cells in culture as well. Thus, high levels of DHA leading to abundant LR11 seem to protect against Alzheimer's, Cole said, while low LR11 levels lead to formation of the amyloid plaques.

Fish oil and its key ingredient, omega-3 fatty acids (found in fatty fish like salmon), have been a mainstay of alternative health practitioners for years and have been endorsed by the American Heart Association to reduce the risk of cardiovascular disease.

Fatty acids like DHA are considered "essential" fatty acids because the body cannot make them from other sources and must obtain them through diet. Years of research have shown that DHA is the most abundant essential fatty acid in the brain, Cole said, and that it is critical to fetal and infant brain development. Studies have also linked low levels of DHA in the brain to cognitive impairment and have shown that lower levels may increase oxidative stress in the brains of Alzheimer's patients.

Based on the positive results, the National Institutes of Health is currently conducting a large-scale clinical trial with DHA in patients with established Alzheimer's disease. For those patients, Cole said, it may be too late in the disease's progression for DHA to have much effect. But he is hopeful that the NIH will conduct a large-scale prevention clinical trial using fish oil at the earliest stages of the disease — particularly because it is unlikely that a pharmaceutical company will do so, since fish oil in pill form is readily available and inexpensive.

Still to be determined, he said, "is what the optimal dose should be. It could be that a smaller amount might be helpful, especially in a place like the south of France, where people are already on a Mediterranean diet."

Here in the United States, though, where fish consumption is not very high, the dose may need to be higher.

"There's a deficiency of DHA to begin with," Cole said, "and this may contribute to the low LR11 seen in many Alzheimer's patients."

That is terrible, if true. He has a beautiful, creative (to the power of 10) mind. He is my favourite author. I go back and read and re-read his books always discovering new things. I have only ever read one other fiction book more then once (Lord of the Rings)

NEW YORK, Nov. 19 (UPI) -- Amyloid beta plaques, a hallmark of Alzheimer's disease, can be prevented by interacting with the protein cystatin C, U.S. and German researchers have found.

Lead author Efrat Levy of the New York University School of Medicine said two animal studies may open the door to new treatments for Alzheimer's disease that mimic the effects of cystatin C.

The first study, by Levy and researchers at the Nathan S. Kline Institute for Psychiatric Research and New York University School of Medicine, and the second study with Levy and colleagues in the laboratory of Dr. Mathias Jucker at the Hertie-Institute for Clinical Brain Research in Tubingen, Germany, used genetically engineered mice to produce human cystatin C and abundant amounts of amyloid beta plaques in their brains.

The protein cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice, and inhibited the aggregation and deposition of amyloid beta plaques in the brain, Levy said.

Both studies are published online in advance of the December print issue of the journal Nature Genetics.

Now this bastard of a disease is getting personal.What can be done?More money for research?

Why does it attack such intelligent vibrant people with so much to offer the world?Terry Pratchett has more ideas and more weird neuron connections to bizarre useless information than anyone on this planet.He is a most neglected and undervalued writer even if he sells more books than anyone else he is still stupidly seen as a cult thing. He has created his own unique and wonderful "genre" and people can't put him in a box.BUT THIS IS TERRIBLE

Welcome to issue 129 and the start of a shiny new year. Unless youlive on another planet you can't have missed the news that Terry hasbeen diagnosed as having a rare form of early onset Alzheimers.Below is what Terry wrote about it on 11th December 2007.

AN EMBUGGERANCE

Folks,

I would have liked to keep this one quiet for a little while, butbecause of upcoming conventions and of course the need to keep mypublishers informed, it seems to me unfair to withhold the news. Ihave been diagnosed with a very rare form of early onsetAlzheimer's, which lay behind this year's phantom "stroke".

We are taking it fairly philosophically down here and possibly witha mild optimism. For now work is continuing on the completion ofNation and the basic notes are already being laid down for UnseenAcademicals. All other things being equal, I expect to meet mostcurrent and, as far as possible, future commitments but will discussthings with the various organisers. Frankly, I would prefer it ifpeople kept things cheerful, because I think there's time for atleast a few more books yet )

PS I would just like to draw attention to everyone reading theabove that this should be interpreted as 'I am not dead'. I will,of course, be dead at some future point, as will everybody else.For me, this maybe further off than you think - it's too soon totell. I know it's a very human thing to say "Is there anything I cando", but in this case I would only entertain offers from veryhigh-end experts in brain chemistry.

Then due to the high amount of traffic he was receiving he updatedthe news with the following on the 12th December.

AN UPDATE

Folks,

My good friend Sandra Kidby of PJSM Prints[http://www.pjsmprints.co.uk] is allowing me to use her websitebecause I am proverbially too busy to run one of my own. We havehardly the time even to read the thousands of messages that havecome in here, let alone reply to them, but thank you all.

Could I make a small comment, however? Lots of people are sendingme plot ideas. Please, I have a lot of ideas. There is no shortageof ideas and ideas sent to me, even with the very best ofintentions, are carefully filleted out of the correspondence beforethey even get to me. I know they are sent in an effort to help, andI appreciate this, but I advise you not to waste your time.

I am also getting a lot of requests for interviews. I am not givingany because everything I have got to say or that can be said is inthe bulletin below. There is no point in saying it again, but in adifferent order.

Can I remind everybody that I still aten’t dead, even today.

Thanks again for all your good wishes.

Discworld Monthly of course wishes Terry all the best and hopes thatthe world will soon leave him alone a bit so that he can get on withwhat he enjoys doing most which is writing books

The following information is a reminder of your current mailinglist subscription:

You are subscribed to the following list: Discworld Monthly

using the following email:xxxxxxxxxxxxxxxxxxxxxxxxxx

You may automatically unsubscribe from this list at any time byvisiting the following URL:

Boosting levels of testosterone in the body can reduce levels of the protein beta amyloid in the brain, one of the key players in causing Alzheimer's disease, according to a recent breakthrough in Australian research. Read Transcript

Some interesting long-term research projects starting in Australia.Professor for Ageing and Alzheimer's disease at Edith Cowan University are excited about their latest study. It's showing a strong link between the male sex hormone testosterone and Alzheimer's disease.. . . . . .One of the things that is quite clear is that obesity is a risk factor for Alzheimer's disease and obesity also results in a reduction of testosterone levels.

******************************

Now meet Joan Mann, who's a volunteer in a large study set up to help us understand what happens when we age.

An extraordinary new scientific study, which for the first time documents marked improvement in Alzheimer’s disease within minutes of administration of a therapeutic molecule, has just been published in the Journal of Neuroinflammation.

This new study highlights the importance of certain soluble proteins, called cytokines, in Alzheimer’s disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a critical component of the brain’s immune system. Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimer’s disease interfere with this regulation. To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimer’s.

Just listened to thisHealth Report - 21 May 2007 - Alzheimer's, testosterone and the ageing brainBig study being done in Australia.Diet is part of it.It only stays podcast on the site for four weeks.If I can workout how to download and upload it I will attach it to this post (big ask)Well worth a listen.Alzheimer's, testosterone and the ageing brainBoosting levels of testosterone in the body can reduce levels of the protein beta amyloid in the brain, one of the key players in causing Alzheimer's disease, according to a recent breakthrough in Australian research.

--This may actually support my theory....Low ambient level testosterone people are more likely to "ponder" upon daily dealings of emotions. -I say ambient, because the opposite effect can occur when either + or - ive swings of Testosterone levels occur (--usually based on the persons actually brain state at the time of the swing ---> so artificially trying to swing the levels may not achieve the desired effect) ,, ie If a person has programmed themselves to ponder, than getting rid of such a childhood nuance from thier current state is near on impossible without MORE pondering.--ie, to get alleviate the process that has cuased the databank detriment, you need to instances the process that caused. The only tweak that you have to add to the new instance is to 'not' store emotion.

Linux Talk:--it's about Killing a Daemon process, specifically the "Data Delegation System"and typing>/etc/rc.3/Data Delegation System --What's Now not Past not Present --restart or more likely what's neede in human terms, yet still in Lunix speak

>/etc/rc.1/Epiphany --reload and get intouch with>/etc/rc.1/Logic --add data < Epiphany Fart Data (Aurora northern Lights style input)>/etc/rc.1/Logic -- link --> Epihany, --start>/etc/rc.2/Standard Worker Process --restart (citing previous epiphany, within each task in higher lever init's) , ie that is to say the Epiphany must be remmeber and not just shoveled into another memory bank... it must spread like a virus throughout the Standar Worker Processes of the daily living of the being.>/etc/rc.3/Data Delegation System --rememeber epihapny, spread to other thoughts/algortihms and link to the reasoning Deamon. Let the reasoning Deamon know that you will not be stroing memory about emotion any longer and can now work on the epiphany data.

.... so how could this be done

--ECT seems to be one option... after a course of ECT the mind has a window to start Anew with it's Daemons... sadly most of the time this isn't the case. - environment would be a crucial issue after the ECT ....

however unorthodox, and probably unethical...

Grab the person... start them off by suggestive Memory maps.... you need to give them time to start typing in the commands to A. Kill the Data Delegation Daemon, B. when re-invoked, to not bother with emotion, and re-instance the Reasoning Daemeon with new Epiphany Data.

Techniques include talking about the possibility of Learning the Piano. - Do all the subconscience mumbo with the patient - ie. actually let them pass by a Piano accidentally.Do all paper work around them in yellow.When you feel that the subconscience has taken on the algrotithm your trying to setup... wait, then start ECT (maybe 3months after)

ECT -- do it, and keep the person in a state of stupor (via drugs, not ECT!!)in the stupor state instantiate the paper work, and the piano... constant piano playing comes to mind, with yellow scores.

Awaken the person... take away the vectors that started the knew logical layer thought process.... make sure NO thoughts about emotional state are instantiated (of course need I remind that during ECT you are to treat the person like a number, so that they finally "get it" --if they seem emotionalduring the stupor state, than nothing you do durin awakening will help)

Now...you have to get them to actually start thier new hobby (the piano)... the reasoning process needs a new avenue to amuse itself. ie. before it was good at reasoning emotion, now it needs to reason why Beethoven was still able to listen deaf.

-the Logic Layer... it's not good enough to flood the system with Piano data... the Data Delegation system is already exhausted. In other words, rope learning the piano won't work (neither will tutoring --to much possibility of starting up emotion reasoning again 00 remeber that the reasoning Daemon asks the Data Delegation System for input.), so the learning has to be Autonomous, the reasoning Daemon must be called by the Data Delegation layer that is taking care of desire.

So things to take from this convoluted theory...

Thier is no emotion (just like a computer) ... thier are only a bunch of Algorithms, that can only work at certain rates (threading/mutiprocessing is limited by physics of the mind -- and the PC!)

The only emotion that we "feel" is that of the Mind getting "hot or cold" , like a CPU gets hot or cold... but in the mind's case it's the chemical resovoir that is the skull that causes these states.... eg. Alchol is like water to the CPU (if the cpu were to say made out of vacuum tubes and not sealed) - difference with the human mind is that little robots come and fix things (to an extent), Sadly the only way to fix things of the mind is to re-work the algorithms. -which maybe impossible if you haven't the source code.

Just listened to thisHealth Report - 21 May 2007 - Alzheimer's, testosterone and the ageing brainBig study being done in Australia.Diet is part of it.It only stays podcast on the site for four weeks.If I can workout how to download and upload it I will attach it to this post (big ask)Well worth a listen.Alzheimer's, testosterone and the ageing brainBoosting levels of testosterone in the body can reduce levels of the protein beta amyloid in the brain, one of the key players in causing Alzheimer's disease, according to a recent breakthrough in Australian research.

--This may actually support my theory....Low ambient level testosterone people are more likely to "ponder" upon daily dealings of emotions. -I say ambient, because the opposite effect can occur when either + or - ive swings of Testosterone levels occur (--usually based on the persons actually brain state at the time of the swing ---> so artificially trying to swing the levels may not achieve the desired effect) ,, ie If a person has programmed themselves to ponder, than getting rid of such a childhood nuance from thier current state is near on impossible without MORE pondering.--ie, to get alleviate the process that has cuased the databank detriment, you need to instances the process that caused. The only tweak that you have to add to the new instance is to 'not' store emotion.

Linux Talk:--it's about Killing a Daemon process, specifically the "Data Delegation System"and typing>/etc/rc.3/Data Delegation System --What's Now not Past not Present --restart or more likely what's neede in human terms, yet still in Lunix speak

>/etc/rc.1/Epiphany --reload and get intouch with>/etc/rc.1/Logic --add data < Epiphany Fart Data (Aurora northern Lights style input)>/etc/rc.1/Logic -- link --> Epihany, --start>/etc/rc.2/Standard Worker Process --restart (citing previous epiphany, within each task in higher lever init's) , ie that is to say the Epiphany must be remmeber and not just shoveled into another memory bank... it must spread like a virus throughout the Standar Worker Processes of the daily living of the being.>/etc/rc.3/Data Delegation System --rememeber epihapny, spread to other thoughts/algortihms and link to the reasoning Deamon. Let the reasoning Deamon know that you will not be stroing memory about emotion any longer and can now work on the epiphany data.

.... so how could this be done

--ECT seems to be one option... after a course of ECT the mind has a window to start Anew with it's Daemons... sadly most of the time this isn't the case. - environment would be a crucial issue after the ECT ....

however unorthodox, and probably unethical...

Grab the person... start them off by suggestive Memory maps.... you need to give them time to start typing in the commands to A. Kill the Data Delegation Daemon, B. when re-invoked, to not bother with emotion, and re-instance the Reasoning Daemeon with new Epiphany Data.

Techniques include talking about the possibility of Learning the Piano. - Do all the subconscience mumbo with the patient - ie. actually let them pass by a Piano accidentally.Do all paper work around them in yellow.When you feel that the subconscience has taken on the algrotithm your trying to setup... wait, then start ECT (maybe 3months after)

ECT -- do it, and keep the person in a state of stupor (via drugs, not ECT!!)in the stupor state instantiate the paper work, and the piano... constant piano playing comes to mind, with yellow scores.

Awaken the person... take away the vectors that started the knew logical layer thought process.... make sure NO thoughts about emotional state are instantiated (of course need I remind that during ECT you are to treat the person like a number, so that they finally "get it" --if they seem emotionalduring the stupor state, than nothing you do durin awakening will help)

Now...you have to get them to actually start thier new hobby (the piano)... the reasoning process needs a new avenue to amuse itself. ie. before it was good at reasoning emotion, now it needs to reason why Beethoven was still able to listen deaf.

-the Logic Layer... it's not good enough to flood the system with Piano data... the Data Delegation system is already exhausted. In other words, rope learning the piano won't work (neither will tutoring --to much possibility of starting up emotion reasoning again 00 remeber that the reasoning Daemon asks the Data Delegation System for input.), so the learning has to be Autonomous, the reasoning Daemon must be called by the Data Delegation layer that is taking care of desire.

So things to take from this convoluted theory...

Thier is no emotion (just like a computer) ... thier are only a bunch of Algorithms, that can only work at certain rates (threading/mutiprocessing is limited by physics of the mind -- and the PC!)

The only emotion that we "feel" is that of the Mind getting "hot or cold" , like a CPU gets hot or cold... but in the mind's case it's the chemical resovoir that is the skull that causes these states.... eg. Alchol is like water to the CPU (if the cpu were to say made out of vacuum tubes and not sealed) - difference with the human mind is that little robots come and fix things (to an extent), Sadly the only way to fix things of the mind is to re-work the algorithms. -which maybe impossible if you haven't the source code.

We have had many tens of thousands of e-mails from people and the letter flood is just beginning to bite (hilariously, spam traps here tend to pick up things like 'medication' and treat quite a lot of the mail as spam. If we switch them off, we get all the spam too - hurrah!). All this good will is appreciated, although there is no way on gods earth that I will be able to reply to even a fraction of you. I would like people to bear in mind that I have been diagnosed quite early after an MRI scan and a whole afternoon of tests. While nothing is certain, one does not have to be unduly optimistic to believe that I will be around and, hopefully, working for some time to come. My advice, therefore, is to calm down and await events. I have not actually gone, yet.

As an aside, thanks to everyone who bought Making Money making it, we understand, the best selling hardback fiction of 2007. At least that's what the figures say. It will be interesting to see if the papers say it too.

East meets West in the search for Alzheimer's therapeutics - novel dimeric inhibitors from tacrine and huperzine A.

Li WM, Kan KK, Carlier PR, Pang YP, Han YF.

Department of Biochemistry, Hong Kong University of Science and Technology, Hong Kong Special Administrative Region, China.

Alzheimer's disease (AD) is linked to cholinergic deficiency and the overactivation of glutamate receptors. The acetylcholinesterase (AChE) inhibition treatment approach has produced the most encouraging results in clinical practice, and memantine, a moderate antagonist of N-methyl-D-aspartate (NMDA) receptors, has been approved for treating AD. However, AChE inhibitors have limited success as they only improve memory in mild dementia but cannot stop the process of neurodegeneration; while memantine possesses neuroprotective effects only with a little ability in memory enhancement. There has been a major rush among neuroscience research institutions and pharmaceutical firms worldwide to search for safer and more effective therapeutic agents for AD. The novel dimers, derived from tacrine and the fragment of huperzine A (HA'), have been demonstrated to be potent and selective reversible inhibitors of AChE. Bis(7)-tacrine, bis(12)-hupyridone (E12E) and HA'(10)-tacrine, are representatives of three series of novel dimers. According to the preclinical studies, these compounds have been shown to have low toxicity and high efficacy for improving cognitive deficits in several animal models. More interestingly, bis(7)-tacrine, similar to memantine, prevents glutamate-induced neurotoxicity by moderately blocking glutamate receptor NMDA subtype. Furthermore, bis(7)-tacrine, as well as E12E, possesses multiple neuroprotective effects in vitro and in vivo. Taking together, these dimeric AChE inhibitors, especially bis(7)-tacrine, E12E and HA'(10)-tacrine, may provide beneficial effects in AD and other neurodegenerative diseases.

Manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedy or dietary supplement.

Ginkgo Biloba. Ginkgo biloba is a common herb that has antioxidant properties and appears to increase blood flow to the brain. A 2002 study of healthy people who took over-the-counter ginkgo for 6 weeks reported no improvements in memory or mental function. Studies are reporting that a ginkgo biloba extract, called Egb 761, may slightly improve the memory of patients with mild to moderate Alzheimer's disease. The herb poses a small increased risk for bleeding, which may be hazardous in combination with other blood-thinning medications, such as warfarin or high-doses of vitamin E.

Turmeric. Studies suggest that circumin, a compound found in the spice turmeric, has properties that may protect against the Alzheimer's disease process.

Melatonin. Melatonin, a natural hormone involved in sleep regulation, is of interest to researchers. It is an antioxidant, may break down beta amyloid, and is able to pass through the blood-brain barrier. Deficiencies have been observed in patients with Alzheimer's disease. A number of studies (but not all) report that melatonin may improve sleep habits in these patients. Some studies reported slower progression of mental impairment.

lots of other things potentiate opiates. antideppressants are notorious. the obvious **** like alcohol and benzo,s ( seems like most OD,s are associated with these, I know mine was.) cats claw herb, and a host of other herbs most likely......memantine, TAGAMET.

Memantine is not available in the US at this time. It is in stage 3 trials for Alzheimerâ€™s disease. US approval may come within the next 2 years. Memantine is now approved in the European Union for the treatment of Alzheimerâ€™s. It has been marketed in Germany since 1978 for the treatment of dementia and other cognitive disorders. It comes in 10mg tablets. One or two tablets/day are sufficient to prevent opiate/amphetamine tolerance, overactivity of the NMDA receptor and consequent free radical stress inside the neuron. The most expensive option though.

ScienceDaily (Jan. 2, 2008) — It's good news that we are living longer, but bad news that the longer we live, the better our odds of developing late-onset Alzheimer's disease.

Many Alzheimer's researchers have long touted fish oil, by pill or diet, as an accessible and inexpensive "weapon" that may delay or prevent this debilitating disease. Now, UCLA scientists have confirmed that fish oil is indeed a deterrent against Alzheimer's, and they have identified the reasons why.

"Part of me lives in a world of new age remedies and science, andsome of the science is a little like voodoo, but science was neveran exact science, and personally I'd eat the arse out of a dead moleif it offered a fighting chance."

On the issue of raising awareness of dementia and the urgent needfor more research, the author added: "I intend to scream andharangue while there is time."

In the unlikely event that you missed the news this month, Terry haspersonally donated 1 million USD to Alzheimers Research UK. Moreinformation about this is included in the news section.

Various fans felt it would be good to "Match it for Pratchett", soif you wish to make a small donation why don't we see if we can(collectively) match Terry's contribution.

Mounting evidence suggests that physical activity may have benefits beyond a healthy heart and body weight. Through the past several years, population studies have suggested that exercise which raises your heart rate for at least 30 minutes several times a week can lower your risk of Alzheimer's. Physical activity appears to inhibit Alzheimer's-like brain changes in mice, slowing the development of a key feature of the disease.

In one observational study, investigators looked at the relationship of physical activity and mental function in about 6,000 women age 65 and older, over an 8 year period. They found that the women who were more physically active were less likely to experience a decline in their mental function than inactive women.

Another compelling study, conducted by researchers at the University of Chicago, was highlighted on ABC News last week. The study used mice bred to develop Alzheimer's type plaque in the brain. In the study, some mice were allowed to exercise and others were not. The brains in the physically active mice had 50 to 80 percent less plaque than the brains of the sedentary mice and they (exercising mice) produced significantly more of an enzyme in the brain that prevents plaque.

I wonder if this research would have benefits for brain disorders like Alzheimer's?

Results

We determined that human umbilical cord blood mononuclear cells (UCBMC) given peripherally, by an intravenous injection, could rejuvenate the proliferative activity of the aged neural stem/progenitor cells. This increase in proliferation lasted for at least 15 days after the delivery of the UCBMC. Along with the increase in proliferation following UCBMC treatment, an increase in neurogenesis was also found in the aged animals.. . .Conclusion

The results demonstrate that a single intravenous injection of UCBMC in aged rats can significantly improve the microenvironment of the aged hippocampus and rejuvenate the aged neural stem/progenitor cells. Our results raise the possibility of a peripherally administered cell therapy as an effective approach to improve the microenvironment of the aged brain.